Endometriosis is a hormone-dependent inflammatory disease that results in the presence of endometrium in the peritoneal cavity. The endometriosis lesions can be superficial or deep and can develop ovarian cysts (endometriomas). The mechanism of formation of such lesions is twofold. Firstly, the eutopic endometrial cells flow back into the peritoneal cavity through the tubes in each menstruation, then these cells, once in the peritoneal cavity, will adhere and invade the peritoneum, proliferate, thereby forming lesions. The proliferation of ectopic endometriotic lesions depends on hormonal factors, particularly local and systemic production of estradiol, and also on the local inflammatory response in the peritoneum and production of trophic factors (cytokines, chemokines, angiogenic factors, prostaglandins) for lesions.
Many molecules that could block the proliferation of endometriosis cells are currently under development. These molecules inhibit the proliferation by acting on the hormonal level and blocking the proproliferative effect of estradiol (aromatase inhibitor or receptors to estradiol, progestins), or by acting on the inflammatory component (antioxidant, prostaglandin inhibitor or pro-inflammatory cytokines), or by blocking intrinsic mitogenic signals endometriotic cells induced by the inflammatory response by inhibiting the MAPK or the mTOR-Akt pathway activated in these cells.
However, it remains a need to explore and understand such mechanism and, therefore, a need to develop new molecules to be applied in efficient treatments for treating and/or preventing endometriosis.